The five chapters in Part 3 of William Lane Craig’s beautifully written book In Quest of the Historical Adam turn to the scientific investigation of human evolution to answer three questions:
- What are the behaviors that make us humans?
- When do we first see these behaviors in geological time?
- What are the scientific objections to concept of one man and one woman giving rise to all humans today?
To answer the first question, Craig takes the reader on a tour of what is known about the origins of language and complex thought, from neurology to artifacts and cave paintings. He concludes that “human behaviors that exhibit modern human cognitive capacity did not originate recently, or even very early, among Homo sapiens alone but were already in place in our last common ancestor with Neanderthals and Denisovans” (p. 329). From the archaeological and paleoanthropological records, Craig derives an answer to the second question, estimating that these behaviors arose between seven hundred and fifty thousand to one million years ago with the species Homo heidelbergensis.
I appreciate the caution with which Craig reviews this literature. He even disagrees with some of the scientists’ conclusions that would have facilitated the search for Adam in a more recent time period. While I agree with Craig’s assessment of the likely intellectual capacity of these earlier people, I would not be so quick to place a specific genus and species name to the dawn of this cognitive ability. Even though some of my paleoanthropological colleagues bicker incessantly as to which fossils are Homo heidelbergensis and which ones are not, species names tell us nothing about the biological lives of these past individuals. Organism do not have genus and species labels affixed to their foreheads, influencing how they interact with other organisms. Biologists invented taxonomic naming in order to facilitate scientific discussion.
Taxonomic names are also problematic because they are static while species lineages change through time. This change is exceedingly gradual and imperceptible at the level of the individual. By definition, mothers always give birth to babies that are members of their same species. And so, where do you draw the line between species in a lineage? Wherever the taxonomist thinks best. This is why my colleagues argue so much. From my perspective, the parcellation of human variation into Homo heidelbergensis, Homo rudolfensis, late Homo erectus, Homo bodoensis, Neanderthals, or Denisovans, etc., is a diversion from the larger behavioral phenomenon explored in this book. Craig’s conclusion—that all of these larger-brained peoples had the cognitive capacity of humans today—has an inclusivity and sense of possibility that is cut short by tying it unnecessarily to just one species name.
Turning to his third question, Craig dives into population genetics. He articulates the reason for this intellectual excursion: “What is crucial here is that any changes introduced into Adam and Eve be heritable, so that they beget another human being” (p. 377). The review of population genetics lacks the breadth of the earlier chapters, and in so doing misses an opportunity to update the concept of heritability. But let’s start with the genetics.
Genomics is a fast-paced research area that adds new insight to human evolution on almost a monthly basis. I do not envy the person attempting to summarize this scientific literature in just twenty pages, especially when attempting to critique the prevailing consensus of humans evolving as populations. Craig’s brief overview addresses six counterpoints from genetics that Joshua Swamidass outlines as incompatible with Adam and Eve (p. 339). Craig critiques each and concludes that these six counterpoints are not valid, and therefore, that it is possible humans derive from just one man and one woman around one million years ago.I appreciate the caution with which Craig reviews this literature.
Perhaps it is the drive for brevity in this section that has Craig adhering so closely to these six points. Consequently, he does not dive into the more recent genomics evidence or what scientists know about viable population sizes from conservation biology and inbreeding that would have provided the same level of skepticism demonstrated in earlier chapters.
For example, when Craig discusses the concept of trans-species variation, or what is also called incomplete lineage sorting, he discusses Francisco Ayala’s example of the variation in the Human Leukocyte Antigens (HLA) gene complex.Francisco J. Ayala, Ananias Escalante, Colm O’Huigin, and Jan Klein, “Molecular Genetics of Speciation and Human Origins,” Proceedings of the National Academy of Sciences 91, no. 15 (1994): 6787–794. The suite of HLA genes, also called the Major Histocompatibility Complex (MHC), is found in all vertebrates and provides the immunological mechanisms that fight off pathogens specifically rather than through general immune responses, such as inflammation and fever. These genes are the blueprint for our acquired immune system, coding for the mechanisms that learn through infection or, these days vaccines, to identify, remember, and mount a strong attack during re-infection of specific pathogens. Having a lot of variation in your HLA gene complex leads to a healthier acquired immune system, but having a lot of recombination in your HLA gene complex invites more opportunity for mutations that could be deleterious. Without a functioning acquired immune system, your ability to survive infection from even a mild cold virus is greatly reduced.Every region of your genome has its own unique evolutionary history depending on what kind of effect the locus has on the organism. Do you remember the story of the “boy in the bubble”?Clyde Haberman, “‘The Boy in the Bubble’ Moved a World He Couldn’t Touch,” The New York Times, December 6, 2015. This is the famous medical case of David Phillip Vetter, who lacked a functioning acquired immune system and died at age twelve from one of the most common human viruses, Epstein-Barr. There is intense selection to maintain genetic variation in the HLA genes and, simultaneously, intense selection to reduce new (unpredictable) mutations from getting introduced.
We see from this overview that the HLA gene complex is not a typical region of the human genome. But that said, every region of your genome has its own unique evolutionary history depending on what kind of effect the locus has on the organism. There has been selection over many millions of years for the HLA genes to be inherited in larger blocks compared to other regions of the genome, and there has been selection to maintain a lot of variation between a person’s two copies of the HLA genes. Consequently, these genes are the most variable across humans. They are so variable that some human HLA alleles are more similar to chimpanzee HLA alleles than they are to other the HLA genes of other humans, a jaw-dropping fact when you first hear it. This is the phenomenon referred to as incomplete lineage sorting. Ayala uses this example to demonstrate that human genetic variation extends too deeply in time for all of humanity to have arisen for one man and one woman after our lineage split from that of chimpanzees (see Craig, pp. 342–50). Craig critiques this example, noting that there are four major HLA variants, and that these four variants could reflect the four different copies of chromosome 6 represented in the genomes of Adam and Eve (two each). Craig writes, “although the issue is still under debate, most studies have failed to uncover evidence of trans-species variation between humans and nonhuman ancestors involving more than four allele lineages” (p. 349).
This conclusion has a disconnect with modern genomics. The HLA genes represent only about four million base pairs on one human chromosome, just one percent of the human genome’s three billion base pairs. When Ayala published his HLA example in 1994, the idea of accessing a multitude of genetic sequences for the other ninety-nine percent of the genome was just a dream. But now there are thousands of human genomes that can and have been analyzed. What do the other nearly three billion base pairs say about incomplete lineage sorting? It turns out that the vast majority of the human nuclear genome coalesces between one million and five million years ago.See David Reich, Who We Are and How We Got Here: Ancient DNA and the New Science of the Human Past (Oxford: Oxford University Press, 2018), 10–15. When Craig says there is no evidence for incomplete lineage sorting beyond the four alleles of HLA, this is only true if you limit your investigation to living species. With whole-genome analyses and the ancient DNA available from people living as far back as one hundred thousand years ago, we have a much better understanding of the evolutionary histories of every locus in the human genome. The HLA genetic variation goes deep into evolutionary time, before the last common ancestor with chimpanzees and humans. Other genomic regions had a last common ancestor who lived during the time of Ardipithecus, a genus of apes who walked on two legs like we do, but who had a chimpanzee-sized brain and an opposable big toe. Incomplete lineage sorting, or transspecies variation for sure. Therefore, if we include a more complete genomic data set, the scientific evidence continues to reject the hypothesis that a pair of people who lived seven hundred and fifty thousand years ago are the sole progenitors of the genetic variation observed across living people today.
Another example is when Craig writes, “even if the ancestral population of hominids leading to human remains constantly above several thousand, it does not follow that there were not at some time exactly two humans who emerged within that population . . . it is entirely possible that at some time in the past the total number of breeding humans was exactly two, even though the total population at the time was much greater” (p. 348). Had Craig had the opportunity to take a deeper dive into the scientific literature,A population limited to just two breeding individuals is not going to survive for long because of the deleterious effects of inbreeding among their descendants. he would have explored the improbability of this from a genetic health perspective. It is widely recognized in biology that there is a minimum size at which a population is viable. A population limited to just two breeding individuals is not going to survive for long because of the deleterious effects of inbreeding among their descendants.
Let’s look at a much less extreme example for comparison, the Spanish Habsburg dynasty (1516–1700). Members of this dynasty wanted to keep their royal power in the family, and so uncle-niece and first cousin marriages were common. These close family relationships ultimately led to an incredibly high prevalence of rare genetic disorders that caused infertility and, ultimately, the end of the reign.Gonzalo Alvarez, Francisco C. Ceballos, and Celsa Quinteiro, “The Role of Inbreeding in the Extinction of a European Royal Dynasty,” PLoS One 4.4 (2009): e5174. The occurrence of rare genetic disorders is common, but the chance that any two people both have the same rare genetic variant is smaller the larger the population size. The smaller the population, the more likely it is that two people who have a child together share the same rare variant. Inbreeding is deleterious because two people in the same family are much more likely to carry the same rare variant in their genomes. How did the initial descendants of Adam and Eve survive the deleterious effects of inbreeding, especially if they were inclined to increasingly self-isolate, as Craig postulates (p. 378)?
An alternative possibility is that other people in the population with Adam and Eve mated with their descendants, negating the inbreeding concern. But this scenario raises another hurdle for the proposal that Adam and Eve are the genetic progenitors of all humans: genetic recombination during the formation of the gametes (egg and sperm cells). Given how the reshuffling of chromosomal regions occurs during gametogenesis, we have many more genealogical ancestors than we do splices of DNA in our genome. For example, if you trace your ancestry back to 1776, you only have genomic sequences from half of your one thousand and twenty-four direct ancestors who lived at the time.Scott Hershberger, “Humans Are All More Closely Related than We Commonly Think,” Scientific American, October 5, 2020. Over the generations, there just are not enough chromosomal splices during recombination to enable you to inherit a genetic contribution from every single one of your ancestors. With this in mind, how would a specific genetic variant gifted from God be maintained through dozens of generations, needless to say the thousands of generations over the last one million years such that everyone would have a copy of it in their genomes?
For me, this raises the question: Why does God’s intervention with Adam and Eve have to be genetic?Irene Adrian-Kalchhauser, Sonia E. Sultan, Lisa NS Shama, Helen Spence-Jones, Stefano Tiso, Claudia Isabelle Keller Valsecchi, and Franz J. Weissing, “Understanding ‘Non-genetic’ Inheritance: Insights from Molecular-evolutionary Coosstalk,” Trends in Ecology & Evolution (2020): Vol 35, issue 12, pp. 1078–1089. If the transmission of humanness must be through DNA sequence, it runs into an awkward disconnect with the genetic evidence. Inheritance can be cultural and it can also be rooted in biological function but not be genetic. Biologists are increasingly discovering the importance of non-genetic inheritance, for example the lived experiences of a grandmother can influence the way genes are expressed in her grandchildren. While I do not agree with Craig that genetic data support humanity deriving from one man and one woman at any point in evolutionary time, I also do not think that a lack of direct genetic evidence should make the existence of Adam and Eve any less believable to those who believe the Old Testament as the word of God.
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